Alterations of ventricular function following a myocardial infarction result from a complex interaction of changes in regional wall properties, global chamber geometry, and fiber architecture. Understanding of the contribution and interplay of these changes has been limited by the lack of load insensitive measures of global and regional function, and the frequent absence of regional shortening data encorporating a complete characterization of three dimensional strain. The purose of this proposal is to define the mechanisms by which alterations in regional wall strain following myocardial infarction are related to global ventricular pressure-volume behavior, and compensatory adjustments to ischemic injury. The study will combine the simultaneous measurement of in situ pressure-volume (P-V) relationships, using a conductance-volume catheter, and regional strain and pressure-strain relationships by tracking the motion of multiple implanted radiopaque markers. Dogs will be instrumented, and following control study of both the global P-V relationships and regional wall strain, will be subjected to a transmural myocardial infarction. Chronic study of the regional and global ventricular responses will be made. Tensor analysis of the strain data will define alterations in principal strain directions and amplitudes. Regional pressure-strain relationships will define changes in diastolic and systolic properties, while chamber P-V relationships will assess the net effects on global ventricular performance. Finally, examination of the chronically infarcted ventricle in an isolated supported heart preparation will help define changes in the mechanics and energetics of the remaining functional myocardium. Understanding the mechanisms of myocardial compensation after infarction has important implications to the clinical management of ischemic heart disease. A better appreciation of the nature and limitations of this compensation will provide insight into the pathophysiology and potential therapy of ischemic cardiomyopathy.